Passive smoking and atherosclerosis - IESC/UFRJ

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Figure 5. Passive smoking collected in the 1975 Washington County Census carried out by the Training Center for Public Health Research and carotid wall thickness measured in 1986-89 as part of ARIC’s baseline visit (n=2,073). Passive smoking (census) in 1975 Carotid Wall thickness (ARIC baseline visit) in 1986-89 (16) What important causality criterion can be partly assessed in the study by Diez- Roux, but not in Howard’s study? (The results of the latter are shown in tables 1 and 2 and Figure 3.) What are the major shortcomings of Diez-Roux’s design which prevent a full assessment of the criterion? When comparing the final study group with ARIC participants not linked to the 1975 census, some differences were noted, as shown in table 3: Table 3. Characteristics of ARIC Participants Not Linked to the 1975 Census and the Study Group in the Analysis by Diez-Roux et al Characteristic (measured at the time of the ARIC baseline visit) ARIC Participants Not Linked to the 1975 Census (n=1139) Study Group (n=2073) Mean Age in years (standard deviation) 51.4 (5.7) 54.9 (5.5) Percentage with High School Education 72.4 70.5 LDL Cholesterol in mg/dl (Standard Deviation) 138.3 (35.9) 139.6 (38.6) Systolic Blood Pressure in mmHg (Standard Deviation) 117.3 (16.7) 119.3 (17.6) Percentage with Diabetes 9.1 8.7 Mean Carotid Wall Thickness in 0.746 (0.188) 0.758 (0.212) mm (Standard Deviation) The characteristics of the 811 ARIC Washington County cohort participants who were linked to the 1975 census, but with missing information on passive smoking or wall thickness were very similar to those of the study group. E8-10
(17) Could these differences have affected the results pertaining to the relationship between exposure to smoke in 1975 and wall thickness in 1987-89? Why or why not? The results of the analysis by Diez-Roux are shown in table 4. Table 4. Crude and adjusted mean carotid wall thickness (mm) by exposure to tobacco smoke, excluding persons with prevalent clinical cardiovascular disease¤, Washington County, 1975 and 1987-89 Exposure status Never Active Smokers: Sample Size Crude Mean (mm) Adjusted mean§ ± standard error (mm) [p-value§§] No ETS 189 0.681 0.696 ± 0.012 ETS 1975 only 65 0.711 0.722 ± 0.021 [0.29] ETS 1987-89 only 250 0.732 0.733 ± 0.011 [0.02] ETS 1975 and 1987-89 219 0.692 0.722 ± 0.012 [0.13] Never Active Smokers Ever Exposed to ETS 534 0.713 0.727 ± 0.007 [0.03] Current active smoking in both 1975 & 1987-89 362 0.776 0.785 ± 0.009 [0.0001] ¤ Myocardial infarction, angina pectoris, stroke, intermittent claudication § Adjusted for age, gender, systolic blood pressure, LDL cholesterol, presence of diabetes, fat intake, physical activity scores, alcohol intake, education, body mass index §§ P value vis-à-vis never active smokers not exposed to environmental tobacco smoke Environmental tobacco smoke (18) Do the results of the study by Diez-Roux et al confirm those of the study by Howard et al? Are the results in table 4 entirely consistent with the hypothesis that intensity of exposure is related to carotid wall thickness? How can the consistency or lack thereof be explained? (19) The results of the adjustment presented in table 4 were based on a multiple linear regression model. Why? E8-11
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Passive smoking and atherosclerosis - IESC/UFRJ

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